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Autoimmune Metaplastic Atrophic Gastritis

By Nimish Vakil, MD, Clinical Adjunct Professor, University of Madison School of Medicine and Public Health

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Autoimmune metaplastic atrophic gastritis is an inherited autoimmune disease that attacks parietal cells, resulting in hypochlorhydria and decreased production of intrinsic factor. Consequences include atrophic gastritis, B12 malabsorption, and, frequently, pernicious anemia. Risk of gastric adenocarcinoma increases 3-fold. Diagnosis is by endoscopy. Treatment is with parenteral vitamin B12.

Patients with autoimmune metaplastic atrophic gastritis (AMAG) have antibodies to parietal cells and their components (which include intrinsic factor and the proton pump H+,K+-ATPase). AMAG is inherited as an autosomal dominant trait. Some patients also develop Hashimoto thyroiditis and 50% have thyroid antibodies; conversely, parietal cell antibodies are found in 30% of patients with thyroiditis.

The lack of intrinsic factor leads to vitamin B12 deficiency that can result in a megaloblastic anemia (pernicious anemia) or neurologic symptoms (subacute combined degeneration).

Hypochlorhydria leads to G-cell hyperplasia and elevated serum gastrin levels (often > 1000 pg/mL). Elevated gastrin levels lead to enterochromaffin-like cell hyperplasia, which occasionally undergoes transformation to a carcinoid tumor.

In some patients, AMAG may be associated with chronic Helicobacter pylori infection, although the relationship is not clear. Gastrectomy and chronic acid suppression with proton pump inhibitors cause similar deficiencies of intrinsic factor secretion.

The areas of atrophic gastritis in the body and fundus may manifest as metaplasia. Patients with AMAG have a 3-fold increased relative risk of developing gastric adenocarcinoma.

Diagnosis of autoimmune metaplastic atrophic gastritis is made by endoscopic biopsy. Serum B12 levels should be obtained. Parietal cell antibodies can be detected but are not measured routinely. The issue of surveillance endoscopy for cancer screening is unsettled; follow-up examinations are unnecessary unless histologic abnormalities (eg, dysplasia) are present on initial biopsy or symptoms develop.

No treatment is needed other than parenteral replacement of vitamin B12.

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